1. Field of the Invention
The present invention relates generally to apparatus and methods for restoring and maintaining an open passage in body conduits, such as blood vessels, which have become stenosed or occluded. More particularly, the present invention relates to a vascular stent for maintaining an open blood flow lumen in blood vessels and for preventing restenosis.
Percutaneous transluminal angioplasty (PTA) and percutaneous transluminal coronary angioplasty (PTCA) procedures are widely used for treating stenotic atherosclerotic regions of a patient's vasculature to restore adequate blood flow. Catheters having an expansible distal end, typically in the form of an inflatable balloon, are positioned in an artery, such as a coronary artery, at a stenotic site. The expansible end is then expanded to dilate the artery in order to restore adequate blood flow to regions beyond the stenosis. While PTA and PTCA have gained wide acceptance, these angioplasty procedures suffer from two major problems: abrupt closure and restenosis.
Abrupt closure refers to rapid reocclusion of the vessel within hours of the initial treatment, and often occurs in patients who have recently suffered acute myocardial infarction. Abrupt closure often results from either an intimal dissection or from rapid thrombus formation, which occurs, in response to injury of the vascular wall from the initial angioplasty procedure. Restenosis refers to a renarrowing of the artery over the weeks or months following an initially apparently successful angioplasty procedure. Restenosis occurs in up to 50% of all angioplasty patients and results at least in part from smooth muscle cell proliferation and migration.
Many different strategies have been proposed to ameliorate abrupt closure and reduce the rate of restenosis. Of particular interest to the present invention, the implantation of vascular stents following angioplasty has become widespread. Stents are thin-walled tubular scaffolds which are expanded in the arterial lumen following the angioplasty procedure. Most commonly, the stents are formed from a malleable material, such as stainless steel, and are expanded in situ using a balloon. Alternatively, the stents may be formed from a shape memory alloy or other elastic material, in which case they are allowed to self-expand at the angioplasty treatment site. In either case, the stent acts as a mechanical support for the artery wall, inhibiting abrupt closure and reducing the restenosis rate as compared to PTCA.
While stents have been very successful in inhibiting abrupt closure and reasonably successful in inhibiting restenosis, a significant portion of the treated patient population still experiences restenosis over time. Most stent structures comprise an open lattice, typically in a diamond or spiral pattern, and cell proliferation (also referred to as intimal hyperplasia) can intrude through the interstices between the support elements of the lattice. As a result, instead of forming a barrier to hyperplasia and restenosis, the stent can become embedded within an accumulated mass of thrombus and tissue growth, and the treatment site once again becomes occluded.
To date, proposed treatments for restenosis within previously stented regions of the coronary and other arteries have included both follow-up balloon angioplasty and directional atherectomy, e.g. using the Simpson directional atherectomy catheter available from Guidant Corporation, Santa Clara, Calif. Neither approach has been wholly successful. Balloon angioplasty can temporarily open the arterial lumen, but rarely provides long-term patency. Directional atherectomy can successfully debulk the lumen within the stent, but typically does not fully restore the stented lumen to its previous diameter because the catheter removes the stenotic material in an asymmetric pattern. Moreover, it has been found that the atherectomy cutting blades can damage the implanted stent. Such adverse effects were reported by Bowerman et al. in Disruption of a coronary stent during atherectomy for restenosis in the December 1991 issue of Catheterization and Cardiovascular Diagnosis and by Meyer et al. in Stent wire cutting during coronary directional atherectomy in the May 1993 issue of Clinical Cardiology. The possibility of such adverse outcomes is likely to limit the application of atherectomy as a treatment for stent restenosis and will probably result in more tentative use of the atherectomy cutter within the stented region when it is applied, leading to less complete removal of the stenosis.
For these reasons, it would be desirable to provide improved apparatus and methods for restoring and maintaining an open passage in blood vessels and other body conduits. More particularly, it would be desirable to provide a vascular stent for maintaining an open blood flow lumen in a blood vessel which inhibits restenosis within the stented region and which facilitates methods for treating restenosis within the stented region. The process of inhibiting or treating restenosis within the stent may be performed automatically by a mechanism within the stent or the process may be initiated by an extracorporeal activation means or, alternatively, the process may be performed by using catheter-based, minimally invasive techniques for removing stenotic material from within the stented region.
2. Description of the Background Art
Although a great deal of attention and effort has been focused on the problem of in-stent restenosis very few workable solutions have actually been proposed. One proposed solution is the use of intravascular radiation therapy at the stented site to inhibit smooth muscle cell proliferation and to reduce the incidence of in-stent restenosis. Examples of this approach include U.S. Pat. Nos. 5,059,166, and 5,545,569. Systems for applying intravascular radiation treatment can be divided into two general categories: a) catheter or guidewire based treatment systems for delivering a radioisotope to the treatment site for short term irradiation of the stented region; and b) radioactive stents implanted at the treatment site for longer term irradiation of the stented region. Radioisotopes used in both of these approaches typically include gamma emitters, such as Iridium 192, which have the properties of high tissue penetration and a long radioactive half-life, and beta emitters, such as Phosphorus 32 and Strontium 90, which have the properties of low tissue penetration and a shorter radioactive half-life. Although initial testing of intravascular radiation therapy for reduction of in-stent restenosis has been promising, no one knows what the long-term benefits or the adverse effects of the radiation treatment will be. However, even in the most optimistic scenarios, intravascular radiation treatment is not expected to completely eliminate in-stent restenosis. This uncertainty, coupled with the inconvenience and the potential hazards to health care workers of handling radioactive isotopes, points out the importance of finding other alternatives to this experimental approach.
Another proposed solution is described in U.S. Pat. No. 5,078,736 wherein energy, such as mechanical, heat or radio frequency energy, is periodically applied to a stent implanted in a hollow body duct to inhibit the growth of tissue through the interstices of the stent. The patent describes the use of this method in the ureter, the biliary ducts, respiratory passages, pancreatic ducts, lymphatic ducts, and the like. It is uncertain what the effect of this approach would be in the vascular system where applying energy sufficient to inhibit cell growth may be enough to also trigger undesirable events, such as coagulation of the blood in the vicinity of the stent.
Yet another approach involves the application of light energy, either in the infrared, visible or ultraviolet region, to irradiate the stent and the surrounding area to inhibit the growth of tissue through the interstices of the stent. This approach, sometimes referred to as photodynamic therapy, may be used independently or as an adjunct to angioplasty and stenting. Examples of this approach are described in U.S. Pat. Nos. 5,454,794, 5,441,497, 5,422,362, 5,419,760, and 5,298,018. Although research is ongoing, photodynamic therapy has not yet proven itself to be effective for prevention of in-stent restenosis.
The disclosures of each of the patents referenced above are incorporated herein by reference in their entirety. Each of the approaches represented by these patents has potential drawbacks and none of these experimental approaches has yet been proven to be completely effective for prevention of in-stent restenosis. Consequently, it remains highly desirable to identify and develop a successful treatment for atherosclerosis that will prevent the problem of in-stent restenosis.